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J Neurophysiol 94: 3743-3750, 2005. First published August 17, 2005; doi:10.1152/jn.00797.2005
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SK Channel Regulation of Dendritic Excitability and Dendrodendritic Inhibition in the Olfactory Bulb

Brady J. Maher and Gary L. Westbrook

Vollum Institute, Oregon Health and Science University, Portland, Oregon

Submitted 28 July 2005; accepted in final form 14 August 2005

Small-conductance calcium-activated potassium channels (SK) regulate dendritic excitability in many neurons. In the olfactory bulb, regulation of backpropagating action potentials and dendrodendritic inhibition depend on the dendritic excitability of mitral cells. We report here that SK channel currents are present in mitral cells but are not detectable in granule cells in the olfactory bulb. In brain slices from PND 14–21 mice, long step depolarizations (100 ms) in the mitral cell soma evoked a cadmium- and apamin-sensitive outward SK current lasting several hundred milliseconds. Block of the SK current unmasked an inward N-methyl-D-aspartate (NMDA) autoreceptor current due to glutamate released from mitral cell dendrites. In low extracellular Mg2+ (100 µM), brief step depolarizations (2 ms) evoked an apamin-sensitive current that was reduced by D,L-2-amino-5-phosphonopentanoic acid. In current- clamp, block of SK channels increased action potential firing in mitral cells as well as dendrodendritic inhibition. Our results indicate that SK channels can be activated either by calcium channels or NMDA channels in mitral cell dendrites, providing a mechanism for local control of dendritic excitability.


Address for reprint requests and other correspondence: G. L. Westbrook, Vollum Institute, Oregon Health and Science University L474, Portland OR, 97239 (E-mail: westbroo{at}ohsu.edu)




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